ENO also potently inhibited both IL-2production (measured by ELISA) and IL-2 responsiveness (measured by CTLL-2 response to IL-2) in a concentration-dependent manner, yet did not inhibit acquisition of IL-2 receptors.

The results revealed that this suppression was the net result of an action of PGE2 on at least two events during lymphocyte activation: (i) a down-regulation of IL-2 receptor development on lymphocytes, quantitated with a radioimmunoassay and radioautography; this was noted in MLC or Con A-stimulated lymphocyte cultures in the presence of decidual cells (reversible in the presence of indomethacin or anti-PGE2 antibody), or PGE2, but not PGF2 alpha; (ii) an inhibition of IL-2production in the MLC, measured with a bioassay using an IL-2-dependent T cell line (CTLL-2) and a recombinant IL-2 standard.

The potent stimulatory effect of PMA on IL-2production by EL-4 cells has been confirmed by measuring 3H-thymidine incorporation by the IL-2-dependent T cell line, CTLL-2, in the presence of conditioned medium (CM) from stimulated cultures.

IFN-alpha alone had no effect on either the IL-2production or apoptosis of MOLT-16 cells, but significantly increased both the IL-2 production and apoptosis in the MOLT-16 cells after phytohemagglutinin (PHA) stimulation as determined by CTLL-2 assay and by flow cytometric analysis using propidium iodide (PI) staining.

The human IL-2 receptor, which was expressed on an IL-2-dependent murine T-cell line, CTLL-2, by cDNA transfection, was shown to be functionally active by blocking the endogenous mouse IL-2 receptor with monoclonal antibodies.

A series of hybridoma cell lines which produce monoclonal antibodies (MAbs) against recombinant human interleukin-2 (rIL-2) have been established by fusion of murine myeloma cell line P3-NS1-1-AG4-1 and spleen cells of BALB/c mice which had been immunized with rIL-2. 48 hybridoma strains were selected by a solid-phase screening method which produced MAbs reacting with IL-2: four MAbs, L-15, L-20, L-34, and L-61, exhibited strong inhibition of the proliferating effect of rIL-2 on IL-2-dependent cell lines, NK7 and CTLL-2.

One alternate protocol describes the detection of IL-2 in samples of human serum or supernatants using CTLL-2 cells, while other alternate procedures describe the detection and quantitation of murine IL-4 using a mutagenized subline of CTLL-2, CT.4S, and the detection of human IL-4 using a derivative of the CT.4S mouse cell line, CT.h4S.

However, while overexpression of Bcl-x(L) can prevent CTLL-2 cells from dying in the absence of IL-2, overexpression of Bcl-x(L) does not impair the ability of CTLL-2 cells to be used for proliferation-based IL-2bioassays.

Interleukin-2-induced protein synthesis was also suppressed in a dose related manner over this THC concentration range, with the hPBL being more susceptible to the suppressive effect of THC than the CTLL-2 cells.

Specifically interleukin-2 (IL-2)-dependent CTLL-2 cells were incubated in short term culture in the presence of IL-2 together with bombesin and two analogues, [Lys3]bombesin and [Tyr4]bombesin in different concentrations.

When the effect of LMS on IL-2 receptor (IL-2R) expression in CTLL-2 cells was examined by a receptor-ligand binding assay involving low levels (10-80 pM) of 125IL-2, a modest increase in the level of IL-2R expression was observed.

Together, one possible scenario is that Dlg1 inhibits cell cycle progression of CTLL-2/Tax1, but Tax1 through altering localization of Dlg1 in cells, overcome the cell cycle inhibition to initiate IL-2-independenttransformation.

As discussed above, inactivation of one of the two PDZ proteins should be essential for IL-2-independenttransformation of CTLL-2 by Tax1, since Dlg1 knockdown did not enhance the frequency of cells transformed by Tax1?

The frequency of proliferating T4 cells was assessed by examining wells microscopically, and the frequency of T4 cells producingIL-2 was assessed by examining the ability of supernatants to support CTLL-2 proliferation.

The cytochrome c-sensitive TCR-expressing hybridoma (2B4) was stimulated with pigeon cytochrome c antigen, anti-CD3 crosslinking, or PMA and ionomycin, in the presence or absence of CP, and the resulting IL-2produced was measured in a bioassay using an IL-2-dependent cell line (CTLL-2).

Low concentrations of cholera toxin B subunit (CT-B), which binds specifically to GM1 ganglioside, greatly inhibited IL-2-stimulated DNA synthesis in the IL-2-dependent cell line CTLL-2, but had no effect on proliferation of HT-2.

OBJECTIVES: To compare serum adiponectin and tumor necrosis factor (TNF)-alpha among patients with viral liver diseases; to investigate associations of serum adiponectin and TNF-alpha with histological or viral characteristics of chronic hepatitis C (CHC); to investigate adiponectin and TNF-alpha alterations during interferon (IFN)-alpha treatment; and to assess the relationship between serum adiponectin and TNF-alpha and response rates to treatment.

When the pairs of chimeric receptors (V(H)-IL-2Rbeta and V(L)-IL-2Rgamma, or V(H)-IL-2Rgamma and V(L)-IL-2Rbeta) were expressed in IL-3-dependent pro-B cell line Ba/F3 and IL-2-dependent T cell line CTLL-2, the cognate antigen HEL induced selective expansion of gene-modified cells in the absence of IL-3 and IL-2, respectively.